Abstract
The pathogenesis of TSE has still not been completely clarified and discussed. In fact, in some animal species, other than neuroinvasion, accumulation of PrPre in extraneural tissues has also been found, suggesting the possibility of concomitant lymphoinvasion. In particular, in experimentally infected mice, the lymphoreticular system and the spleen are infected for a long before neuroinvasion. Moreover, infection can be detected in the spleen 1 hour after intraperitoneal infection, suggesting that amplification of the pathogen in the spleen is necessary before neuroinvasion, at least for some scrapie strains (Beringue et al., 2000). In a study on prion diffusion in the hamster model, in animals intraperitoneally (i.p.) infected with the scrapie strain 263K, it was possible to identify a small amount of PrPres in the spleen of the hamsters. Nevertheless, the concentration of PrPres in the spleen showed no correlation with the level of PrPres accumulation in any segment of the brain tissue. According to the authors, the spleen appeared to play a potential but non-essential role in pathogenesis after intraperitoneal infection in the hamster model (Baldauf et al., 1997). The aim of this work was to improve and validate an extraction method useful for quantification of the PrPres in the spleen of prion-infected hamsters.
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